[Update in the clinic of addictions: learning and dopamine]

There are two parallel explanatory models for addictions. One is the homeostatic model, that explains tolerance and the abstinence syndrome. Tolerance and abstinence are reversible phenomena that mask sensitization. These appear more commonly with the continued use of drugs, and are based in the up-regulation of cyclic AMP. The other is the plasticity model, that explains sensitization and compulsive use of drugs or addiction. Addiction is probably irreversible, underlies tolerance, appears more frequently with intermittent use of drugs, and is based in learning and memory mechanisms. Both are boldly linked to environmental and behavioral elements. In the plasticity model, dopamine (DA) has an outstanding role. Its phasic discharge is a temporal reward prediction error marker. It is the prediction error that generates learning. All the addictive drugs provoke a very strong increase of phasic DA discharge in some cerebral nuclei by direct or indirect paths. This increase is interpreted by cerebral circuits as prediction errors that generate learning behaviors. Pavlovian and operating type learning is involved. It is clinically observed as the prominence of environmental cues that are related to drug consumption, and the appearance of behaviors directed to the search and use of drugs, that are mainly involuntary and triggered by these cues. Pleasure (primary reinforcement) plays a role in this model, only in the initial stages of addiction. Understanding this double parallel model allows to design therapeutic interventions directed towards a conscious control of involuntary, environmental and affective cues that trigger drug search and use.